Blunt Cerebrovascular Injury

Introduction

• BCVI is defined as nonpenetrating injury to the carotid or vertebral arteries. It is a rare but morbid complication of trauma if missed on initial survey due to the high risk of stroke.
  • Stroke rates are significantly lower in patients treated for BCVI compared to those who are untreated.
• Many patients may present either asymptomatically or following a polytrauma with multiple critical injuries. Providers should utilize a standardized system, such as the expanded Denver criteria (see below) and/or guidance from the Advanced Trauma Life Support course, to determine whether a diagnostic evaluation is warranted.
• Pathological changes of vessels include intimal dissection, arterial laceration, arterial aneurysm, pseudoaneurysm formation, and complete transection.
• Recent studies have shown an increased incidence of BCVI of up to 1-3% of polytrauma patients compared to those in the past, likely in part due to advancements in imaging technology and more liberalized screening criteria.^1,2

Mechanisms of Injury

• Mechanisms of BCVI may be classified into high-energy traumas that result in extreme rotation and hyperextension of the head and neck, which stretch the vertebral and internal carotid artery (specifically over vertebrae C1-C3), direct blunt trauma to the neck, or compression of a vessel against osseous structures (Table 1).

• In the United States, motor vehicle collisions account for more than 50% of injury mechanisms.³ One of the other most common mechanisms of injury is a fall. While most falls occur from heights, it is also important to consider ground-level falls in the elderly population.
• The type of injury (e.g., near hanging, fall from height) can independently serve as a risk factor for BCVI, separate from the presenting signs and symptoms.
• Cervical spine injuries most commonly lead to BCVI screening, and most but not all BCVIs are associated with cervical spine fractures. There is a strong association between cervical spine injuries and vertebral artery injuries.^1,2

Screening Criteria

• Before protocolized screening, patients with BCVI were often only identified after suffering from stroke and devastating neurological injury.
• Several professional organizations and research groups have put forth and recommended screening criteria, which have undergone multiple iterations over time.
• As screening is both noninvasive and highly accurate, many institutions have liberalized their protocols in an attempt to find the optimal threshold between sensitivity and specificity for BCVI identification.
• While protocols remain institution-dependent, level 1 trauma centers often utilize the expanded Denver criteria to identify patients with BCVI. Most recently, the screening method was expanded to include cervical spine fracture patterns. Any of the findings of the expanded Denver criteria (Table 2) should prompt emergent diagnostic evaluation for BCVI with computed tomography (CT) or magnetic resonance imaging (MRI) angiography.

• The 11th edition of the Advanced Trauma Life Support Course Manual lists the following in addition to the above criteria:
  • Head or cervical CT, done because of the injury mechanism
  • Traumatic brain injury with thoracic injuries
  • Oculosympathetic palsy or Horner’s syndrome
  • Skull fracture involving the petrous temporal bone, carotid canal, base of skull, frontal bone, sinuses, or orbit
  • Neck injury, seatbelt sign, crepitus
  • Blunt cardiac rupture

Diagnostic Evaluation and Grading of Injury

• In patients meeting one or more of the screening criteria, radiologic evaluation should be performed. If an injury is identified, it should be classified using the Biffl injury grading scale (Table 3).
• In the past, digital subtraction angiography (DSA) was considered the gold standard for detecting BCVI. However, this method has been largely replaced by CT angiography (CTA) given improvements in CT channel technology.⁵
  • DSA requires insertion of a catheter into an artery and then guidance into the brain vessels. Images are taken both before and after dye injection, and a computer digitally subtracts the background to create images of the blood vessels. As this is more invasive, it carries a higher risk of procedure-related complications than CTA. Risks include stroke, pseudoaneurysm, and hematoma at the site of vessel puncture.⁵
  • Additionally, a study by Eastman et al. found that using CTA instead of DSA reduced the time from admission to diagnosis from an average of 31.2 hours to 2.65 hours, and that stroke rates for BCVI were reduced from 15.2% to 3.8%.⁶
• MRI technology remains impractical for diagnosing BCVI due to its time-consuming nature and comparable sensitivity and specificity to CTA.
• Critics of widespread screening believe there is a risk of over-triage and unnecessary radiation exposure.5 However, trauma organizations are generally in agreement that the risks associated with CTA are low compared to the potential risk of missing the diagnosis of BCVI.²

Pathophysiology of Injuries

• Stretching or impingement of vessel walls due to forceful flexion, extension, or rotation of the head and neck may result in intimal tears. This serves as the primary pathological mechanism for luminal narrowing, dissection, intramural hematoma, pseudoaneurysm, and embolization. Otherwise, there may be direct laceration of vessels, typically caused by bone fragments, which can result in total or partial transection.
• Intimal Injuries
  • In dissection, luminal blood enters the defect in the intimal layers and propagates cranially. As the false lumen expands, it can narrow and occlude the true lumen of the vessel.
  • Irritation of the intima can also expose thrombogenic collagen, leading to platelet plug formation and the proliferation of emboli that may migrate to intracranial vessels.⁵
• Adventitial Injuries
  • Hemorrhage into the adventitia of an artery without a tear in the intima can result in an intramural hematoma.
  • A localized sac-like outpouching may form in the adventitia as blood leaks from an injured vessel wall, forming a pseudoaneurysm that is at risk of rupture.

Treatment and Management in the Operating Room

Treatment Options

• Treatment options include observation, antithrombotic (ATT) medications, open surgical repair, and endovascular therapy.
• When considering treatment, physicians must consider the patient’s characteristics, symptoms/physical presentation, the location of the injury, as well as the injury grade.
• Generally, observation is not chosen unless there are absolute contraindications to all alternatives, as progression to stroke can result in devastating functional outcomes.
• Grade V injuries carry a high risk of mortality and demand immediate repair. This may be via open surgery or endovascular therapy if the lesion is inaccessible.1 Open surgical repair is often unattainable if the carotid injury is near the skull base.
• When there is severe vessel narrowing or an enlarging pseudoaneurysm, interventional radiologists may choose to place stents to maintain patency.
  • A review of multiple studies has determined a clinically significant rate of stent complications, including dislodgment of unstable thrombus and stent occlusion.¹
  • The Eastern Association for the Surgery of Trauma specifically recommends against routine endovascular stenting for grade II and III BCVIs because the benefits do not outweigh the risks, which include in-stent thrombosis and subsequent stroke. They additionally state that invasive stenting requires long-term ATT, and pharmacologic monotherapy already decreases risk for stroke and mortality.²
  • If the surgical team chooses stent deployment, patients must receive poststent ATT and vigilant monitoring.

ATT Therapy

• The choice of anticoagulant/antiplatelet therapy is based on the severity of the vessel injury and the clinical situation. Studies have shown antiplatelet agents to be equivalent to systemic anticoagulation.³
• Early reports recommended systemic anticoagulation with heparin, no bolus, with a target partial thromboplastin time of 40-50 seconds. More recent reports suggest no difference in efficacy between systemic heparinization and antiplatelet therapy (clopidogrel 75 mg daily or aspirin 325 mg daily) in preventing strokes.¹
• Whether patients with low-grade injuries require long-term ATT, and what the optimal drug regimen and duration should be, is still undetermined.
• A follow-up imaging study is recommended 7 to 10 days after the initial injury and for any change in neurologic status.1 While many grade I and II injuries improve or resolve over time, it is essential to monitor higher-grade injuries to determine whether therapy needs to be modified.

Anesthetic Management

• Physiologic goals when managing these patients include protecting the brain from secondary injury by preventing hypoxia, hypocarbia, hyper or hypoglycemia, hyperthermia, and hypotension.
• The patient’s coagulation status will be managed in consultation with vascular surgery, interventional radiology, and the trauma team. Blood pressure goals for the case need to be communicated between all members of the operating team to facilitate repair.
• Management of other critical injuries with possibly conflicting physiological needs should be kept in mind, and the most lethal injury should be managed first.
• BCVI is rare and may be missed during the initial trauma evaluation. A patient with an undetected BCVI can have a stroke while under anesthesia care while undergoing surgery for another injury. This can result in an abnormal neurological exam upon discontinuation of the anesthetic at the end of the procedure.
• Anesthesiologists can advocate for screening if they are aware of the risk factors for BCVI.

Pediatric Patients

• In contrast to adults, in whom a very liberal screening strategy is employed for BCVI, radiological exposure in children involves a greater risk of developing a malignancy over their lifetimes when exposed to radiation in childhood. Therefore, screening for BCVI is more selective. The Utah score and the McGovern Score systems (Table 4) have been validated, with the former having a sensitivity of 52.4% and the latter 81%. In children, a GCS less than 8 increases the risk of BCVI.¹⁰